Just as the thermostats in our homes keep the temperature at a steady, comfortable level, a ‘thermostat’ in our brain controls the rate of neuron firing. Scientists at #Brandeis University have now demonstrated this ‘thermostat’ at work in rats. Their work shows #neocortical neurons controlling higher functions like sight and spatial reasoning fire at a constant rate, regardless of whether the animal is asleep or awake and that neurons return to this pre-set firing rate even after stimulus is removed. The base firing rate of neurons is set early in life, largely in response to environmental factors.In this work published in Neuron, the neuron firing rate in rats that had temporarily lost vision in one eye initially slowed after having lost some external visual stimulation. But after 48 hours, the neuron firing rate returned to a normal level, as the brain’s ‘thermostat’ worked to return the brain to #homeostasis. And while the patterns of neural firing changed based on whether the brain hemisphere was receiving visual input or the animal was sleeping, rates of neuron firing remained the same. The researchers say that these results could have profound implications for our understanding of diseases like #epilepsy, where neuron firing rates are significantly altered.

“I think every single person perceives things differently. We are all singular.” ~ Julia Leigh

If you’ve ever dropped a tiny pebble into a glass-smooth lake, you know that this single change can reverberate out from the middle of the body of water to the furthest reaches close to shore. It turns out that a single neuron can change a person’s brain waves just like that pebble. Recent research from Yang Dan at the University of California, Berkeley, has uncovered new information about just how powerful an individual neuron is in changing our brain chemistry.

Even though there are thousands of neural connections happening in our brains at any one moment in time, a veritable orchestra of cross-talk and communication, an individual brain cell has much more clout than was previously assumed. We know that the chaotic ways in which the brain communicates to itself and the rest of the body can lead to some pretty serious health issues – starting with insomnia and even sleepwalking, and, later on in life, dementia and other illnesses if left untreated. But we can make changes to these deleterious patterns starting with just one neuron.

As Yang Dan tells us, “A single neuron has more weight than we used to think.” Usually, we look at brain waves – the collection of billions of cells talking to one another through electrical impulses across the brain at large. These patterns can help to control everything from our respiratory rates, to how we respond to a traffic accident, or how we express pleasant surprise when someone buys our coffee in line ahead of us.

This collection of brain wave chatter forms a sine wave, called a brainwave. There are different types of waves, depending on the prevalent type of communication happening between the billions of neurons. For example, large, slow brain waves are associated with deep sleep. During REM or rapid eye movement sleep, another type of wave forms, since there is an overarching change in the flavor of communication happening in the brain at that time, and the communication is less synchronized. There are smaller and more frequent oscillations in the sine waves. When we are awake, the pattern gets even more chaotic, with the neurons chattering like rambunctious school children, broadcasting an uncoordinated, rapid-fire cacophony of electrical signals.

Dan and his colleagues came to their findings by studying how large-scale brain wave patterns influenced a connection between two singular neurons, knowing that repetitive patterns create groove-like electrical pathways that could get stronger over time. When used less often, like grass growing over a walking path, the neuronal pathways become less prominent. Dan and his scientific peers wondered if the overall pattern of brain activity altered the ability of nerve cells to broadcast with a louder decibel, or, so to speak, greater strength.

Using anesthetized rats to produce experiment results, they found that tickling just one neuron in the brain caused a whole set of neurons to fire, even when the surrounding neurons were left undisturbed.

Dan explains the results of his study, “Every neuron makes connections to roughly 1000 other neurons, but most of those are quite weak . . .” What makes this single neuron stimulation firing other areas of the brain interesting is that a target cell won’t normally respond unless quite a few of the neurons that connect to it are stimulated. It usually takes a group effort on the part of cells to get an entire brain wave going. What is odd is that single neurons were found to change the activity of the entire brain, though.

Dan and his team still don’t understand exactly how one cell could exert so much influence over the rest of the brain. They had to repeatedly stimulate a cell to cause a pattern to switch, so it is possible that they were emulating the effect of many cells firing concurrently, although a neuron does not normally fire that way. It is still a question as to whether the activity of the single neuron could change the entire brain pattern under more normal circumstances.

These findings do, however, alter the way scientists understand how patterns are established in the brain. They already know that certain brain structures, like the brain stem and hypothalamus, help to set the tone of the conversations happening in the whole brain, but it turns out that altering just small parts of the brain may have a profound effect on what the brain ‘says’ to us overall. These changes can originate in all areas of the brain, even the corpus callosum, the thin layer between the hemispheres.

We already know that sound, meditation, or even sitting by ocean waves can alter our brain wave patterns so that we exist in a more peaceful state, but it turns out that the change may start from a smaller seed of thought, a single cell firing, than was tacit before this type of study.

Scientists have recorded how the brain changes when it learns something new and forms fresh memories.

The study shows how the brain’s memory system works – and may even lead to the eradication of some phobias and conditions like dementia, according to a Swiss-based research team comprising of Italian, German and Swiss neuroscientists.

Since some memories, such as fears, can leave an intense permanent trace, the research could pave the way for discovering the molecular foundations of phobias and anxieties.

Changes: The researchers recorded how new synapses are formed and pre-existing ones are lost when the brain learns something new

Brain specialist Dr Piergiorgio Strata said: ‘Some of them are sent to permanent storage areas located in various parts of the brain’s cortex, while others are organised differently with inhibitory synapses coming into play.

‘When we have to memorise something, in a structure called the hippocampus or the cerebellum – the things to be remembered are selected.’

The pictures have shown for the first time how memory works by observing how the brain modifies its structure and organisation in order to remember.

When the brain recalls something, neurons lengthen their spindly arms, called axons, to communicate with one another and establish new contacts, or synapses.

In other cases, connections are cancelled out.

The brain is able to recall very quickly certain memories such as fears, as the ‘memory’ has left a strong permanent trace.

‘We can see that short-term memory can become long-term via a process called consolidation, which is completed over several days,’ added Dr Strata.

He continued: ‘The research has supplied ground breaking information on memory function and has paved the way for us to further discover the molecular foundations of phobias and anxieties.’

When Geoffrey Murphy, Ph.D., talks about plastic structures, he’s not talking about the same thing as Mr. McGuire in The Graduate. To Murphy, an associate professor of molecular and integrative physiology at the University of Michigan Medical School, plasticity refers to the brain’s ability to change as we learn.

Murphy’s lab, in collaboration with U-M’s Neurodevelopment and Regeneration Laboratory run by Jack Parent, M.D., recently showed how the plasticity of the brain allowed mice to restore critical functions related to learning and memory after the scientists suppressed the animals’ ability to make certain new brain cells.

The findings, published online this week in the Proceedings of the National Academy of Sciences, bring scientists one step closer to isolating the mechanisms by which the brain compensates for disruptions and reroutes neural functioning — which could ultimately lead to treatments for cognitive impairments in humans caused by disease and aging.

“It’s amazing how the brain is capable of reorganizing itself in this manner,” says Murphy, co-senior author of the study and researcher at U-M’s Molecular and Behavioral Neuroscience Institute. “Right now, we’re still figuring out exactly how the brain accomplishes all this at the molecular level, but it’s sort of comforting to know that our brains are keeping track of all of this for us.”

In previous research, the scientists had found that restricting cell division in the hippocampuses of mice using radiation or genetic manipulation resulted in reduced functioning in a cellular mechanism important to memory formation known as long-term potentiation.

But in this study, the researchers demonstrated that the disruption is only temporary and within six weeks, the mouse brains were able to compensate for the disruption and restore plasticity, says Parent, the study’s other senior author, a researcher with the VA Ann Arbor Healthcare System and associate professor of neurology at the U-M Medical School.

After halting the ongoing growth of key brain cells in adult mice, the researchers found the brain circuitry compensated for the disruption by enabling existing neurons to be more active. The existing neurons also had longer life spans than when new cells were continuously being made.

“The results suggest that the birth of brain cells in the adult, which was experimentally disrupted, must be really important — important enough for the whole system to reorganize in response to its loss,” Parent says.

ScienceDaily (Feb. 28, 2011) — The so-called reward center of the brain may need a new name, say scientists who have shown it responds to good and bad experiences. The finding, published in PLoS One, may help explain the “thrill” of thrill-seeking behavior or maybe just the thrill of surviving it, according to scientists at Georgia Health Sciences University and East China Normal University.

Eating chocolate or falling off a building — or just the thought of either — can evoke production of dopamine, a neurotransmitter that can make the heart race and motivate behavior, said Dr. Joe Z. Tsien, Co-Director of GHSU’s Brain & Behavior Discovery Institute.

Scientists looked at dopamine neurons in the ventral tegmental area of the mouse brain, widely studied for its role in reward-related motivation or drug addiction. They found essentially all the cells had some response to good or bad experiences while a fearful event excited about 25 percent of the neurons, spurring more dopamine production.

Interestingly neuronal response lasted as long as the event and context was important, Tsien said. Scientists used a conditioned tone to correlate a certain setting with a good or bad event and later, all it took was the tone in that setting to evoke the same response from the dopamine neurons of mice.

“We have believed that dopamine was always engaged in reward and processing the hedonic feeling,” Tsien said. “What we have found is that dopamine neurons also are stimulated or respond to negative events.”

Just how eating chocolate or jumping off a building induces dopamine production remains a mystery. “That is just the way the brain is wired,” Tsien said. He notes that genetics can impact the number of cells activated by bad events — and while interpretation of the findings needs more work — they could help explain inappropriate behaviors such as drug addiction or other risky habits.

In a second paper in PLoS One, Tsien and his colleagues at Boston University have provided more insight into how brains decide how much to remember good or bad. Inside the hippocampus, where memory and knowledge are believe to be formed, recordings from hundreds of mouse brain cells in a region called CA1 showed all are involved in sensing what happens, but not in the same way.

They found among most cells a big event, such as a major earthquake, evoked a bigger sensory response than a mild earthquake. But slightly less than half the cells involved logged a more consistent neural response to all events big and small. These are called invariant cells because of their consistent firing regardless of event intensity. Tsien said these cells are critical in helping the brain remember those events.

The initial muted sensory response was followed by the cells replaying what they just experienced. It’s that reverberation that corresponds with learning and memory. “If they play it over and over, you can remember it for a long time,” Tsien said of these memory makers.

But these invariant cells vary in that some keep replaying specific memories while the majority focus on more general features of what occurred. “The general-knowledge cells have the ‘highest volume,'” Tsien said. “So we walk away with general knowledge that will guide your life, which is more important than the details.”

As with the number of dopamine cells that respond to bad or risky behavior, genetics likely plays a role in an individual’s specific ratio of cells involved in encoding general versus more detailed memories, Tsien said. A person with a photographic memory likely has more of the specific memory makers while those with autism or schizophrenia, who have difficulty coping in society, may have fewer of the general memory makers that help provide correct context and understanding of complex relationships.

Turmeric has been used for centuries as part of traditional Indian Ayurvedic medicine, and many laboratory studies suggest one of its components, curcumin, might have various beneficial properties.

However, curcumin cannot pass the “blood brain barrier” which protects the brain from potentially toxic molecules.

The US researchers, who reported their results to a stroke conference, modified curcumin to come up with a new version, CNB-001, which could pass the blood brain barrier.

The laboratory tests on rabbits suggested it might be effective up to three hours after a stroke in humans – about the same time window available for current “clot-busting” drugs.

Chain reaction

Dr Paul Lapchak, who led the study, said that the drug appeared to have an effect on “several critical mechanisms” which might keep brain cells alive after a stroke.

This is the first significant research to show that turmeric could be beneficial to stroke patients by encouraging new cells to grow and preventing cell death after a stroke”Dr Sharlin Ahmed,The Stroke Association

Although strokes kill brain cells by depriving them of oxygenated blood, this triggers a chain reaction which can widen the damaged area – and increase the level of disability suffered by the patient.

Dr Lapchak said that CNB-001 appeared to repair four “signalling pathways” which are known to help fuel the runaway destruction of brain cells.

However, even though human trials are being planned, any new treatment could still be some time away.

Dr Sharlin Ahmed, from The Stroke Association, said that turmeric was known to have health benefits.

She said: “There is a great need for new treatments which can protect brain cells after a stroke and improve recovery.”

“This is the first significant research to show that turmeric could be beneficial to stroke patients by encouraging new cells to grow and preventing cell death after a stroke.

“The results look promising, however it is still very early days and human trials need to be undertaken.”